ReviewFrontiers in microbiology2025
Unveiling the impact of non-coding RNAs on virus-induced cellular autophagy: roles and research advances.
Review in Frontiers in microbiology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
1 citing paper in PubMed.
Corrections and comments
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Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Autophagy is the process by which cells degrade and recycle damaged organelles and macromolecules by forming autophagosomes. This process is closely related to the maintenance of cellular homeostasis, ontogeny, and the occurrence and development of various diseases. Non-coding RNAs (ncRNAs) are a class of RNA molecules that do not encode proteins but play crucial roles in regulating gene expression. Numerous studies have demonstrated that ncRNAs are involved in regulating autophagy, and accumulating scientific evidence suggests that ncRNAs play an essential role in virus-induced cellular autophagy. ncRNAs affect autophagy by participating in the autophagy regulatory network, mediating the transcriptional and post-transcriptional regulation of autophagy-related genes. This review aims to explore the role of ncRNAs in autophagy induced by viral infection and analyze the relevant molecular regulatory mechanisms underlying autophagy. By examining the content above, we speculate that targeted regulation of ncRNAs can affect autophagy induced upon viral infection, thereby achieving antiviral effects and host cell protection.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.